Euthyroid Autoimmune Thyroiditis: Physiopathology of a Still Incurable Disease

Euthyroid Autoimmune Thyroiditis

Last Updated on 21 June 2024

Euthyroid autoimmune thyroiditis, also known as Hashimoto’s thyroiditis, is an autoimmune disorder that affects a large part of the human population.

But, despite all this, it is still a neglected condition. No treatment is available for an autoimmune disease that, even with a normal level of thyroid hormones and abnormal thyroid antibodies, may cause a long series of severe symptoms and discomfort. Why does this happen? This article sheds light on the true causes and physiopathology of euthyroid autoimmune thyroiditis.

Euthyroid Autoimmune Thyroiditis. What Is It?

Euthyroid autoimmune thyroiditis is an autoimmune disorder characterized by a massive attack of the immune system against the thyroid gland. In short: the immune system produces antibodies mistakenly targeted to damage this important endocrine gland. Unlike other types of autoimmune thyroiditis, in the euthyroid autoimmune thyroiditis the level of the thyroid hormones (TSH, FT3 and FT4) may remain normal for your entire life, without causing the final stage of the disease made of hypothyroidism or hyperthyroidism.

However, euthyroid autoimmune thyroiditis is not less severe than other autoimmune conditions, because this disease shares the symptoms of both hypothyroid and hyperthyroid autoimmune diseases.

Indeed, alternatively, you’ll have anxiety, irritability, insomnia, weight loss and tachycardia due to hormone thyroid excess, as seen in hyperthyroidism, and depression, fatigue, and weight gain due to hormone thyroid deficiency, as seen in hypothyroidism.

These symptoms occur even though the thyroid hormones are normal, when you are in the so-called condition known as euthyroid.

Euthyroid Autoimmune Thyroiditis: An Overview on The Missing Treatment

As already said in the introduction, no treatment is available for the autoimmune thyroiditis with an euthyroid condition; namely, when the thyroid produces normal levels of hormones, even if it is inflamed.

Unfortunately, the hormones released by an inflamed thyroid are not always capable of working properly. Once, an immunologist said to me that an euthyroid autoimmune thyroiditis is like a person who has excruciating tooth pain. This person will never be able to perform the daily tasks until the tooth pain is not relieved.

In the case of euthyroid autoimmune thyroiditis, the pain is represented by the inflammation triggered by the immune system and confirmed by abnormal levels of thyroid antibodies.

In Hashimoto’s thyroiditis, the thyroid antibodies are ABTG (antithyroglobulin) and ABTPO (anti-thyroid peroxidase antibodies). According to modern endocrinology, the presence of these serum antibodies is predictive of a future thyroid dysfunction. But, very often, a patient with autoimmune thyroiditis will be euthyroid for the lifetime. This autoimmune disorder is chronic, indeed.

In this case, the endocrinologist won’t prescribe the thyroid hormone replacement, but food supplements to address the nutrient deficiencies that underlie an euthyroid autoimmune thyroiditis.

Most of the time, in fact, euthyroid autoimmune thyroiditis is caused by nutrient deficiencies, such as Vitamin D and Selenium. But there may be other possible causes of this disease, and, often, these causes have nothing to do with the thyroid gland.

Underlying conditions for Euthyroid Autoimmune Thyroiditis

In addition to nutrient deficiencies, other underlying causes of euthyroid autoimmune thyroiditis are: food intolerances, depression and celiac disease.

In most of the cases, however, euthyroid autoimmune thyroiditis has genetic roots and is frequently transmitted to offspring, from parents (often the mother).

Only recently, a study published in Nature and the European Journal of Clinical Nutrition revealed that euthyroid autoimmune thyroiditis may be caused by impaired assimilation of carbohydrates.

During a test performed on 45 participants with euthyroid Hashimoto’s disease, gastrointestinal symptoms have been reported after the administration of lactose, fructose, sorbitol and other carbohydrates, suggesting the evidence of an impaired carb assimilation in this type of patients.

The study, in fact concluded that “carbohydrate malassimilation and gastrointestinal complaints are frequent in euthyroid patients with HT, leading to novel clinical and pathophysiological considerations and concepts.

But it remains to clarify the role of anti-thyroid antibodies on the overall wellness of the patient affected by euthyroid autoimmune thyroiditis. What is their impact on other organs and districts of the body? Euthyroid autoimmune thyroiditis may have an impact on other important organs, such as the gut and brain. Let’s start from the brain.

Impact of Euthyroid Autoimmune Thyroiditis on the Brain

thyroid and brain

It is not clear, yet, which is the pathological role played by the anti-thyroid antibodies on this vital organ, but a clinical trial performed in 2018 on mice revealed that euthyroid Hashimoto’s thyroiditis induces neuroinflammation, because it alters the signal on transmission of serotonin in the brain.

The cause of neuroinflammation seems to be linked to the only anti thyroid peroxidase antibodies, but the inflammatory mechanism needs further exploration.

During the study, “the mice displayed more anxiety- and depressive-like behaviors than controls. Euthyroid Hashimoto’s Thyroiditis mice further showed microglia and astrocyte activation in the frontal cortex”. Microglia and astrocytes are the antibodies of the immune system of the brain.

Even this inflammatory process in the brain has genetic roots. The above-mentioned study showed, in fact, that, in euthyroid Hashimoto’s thyroiditis, there are genes that activate proinflammatory cytokines in the serotonin system. The involved genes are IDO1 and SERT.

The study concluded that euthyroid autoimmune thyroiditis induces neuroinflammation and alters related serotonin signaling in the euthyroid state, which may underlie the deleterious effects of this condition on emotional function.

This finding, hence, explains because euthyroid patients with Hashimoto’s thyroiditis experience psychiatric and emotional symptoms more than in other types of patients.

In a nutshell, the main impact of euthyroid autoimmune thyroiditis is in the brain and on the mood.

Euthyroid patients with autoimmune thyroiditis may, in fact, experience mood swings, anxiety, depression, and severe mental illnesses.

Euthyroid autoimmune thyroiditis has, therefore, the power of dysregulating and upregulating the system that controls the emotions.

That is why patients with autoimmune thyroiditis in the euthyroid stage have trouble tolerating stress. The latter, indeed, is closely tied to the activity of neurotransmitters in the brain. If these neurotransmitters are chronically impaired, stressful events may trigger emotional symptoms, such as extreme fatigue and anxiety.

Often, with Hashimoto’s disease, euthyroid patients who experience chronic fatigue think they have problems with the adrenal glands, especially with cortisol, a hormone which is produced just by these endocrine glands. But, nearly always, the adrenal tests result normal, because the real problem resides in the neuroinflammation caused by the autoimmune disease, not in the thyroid or adrenals.

I lived this experience in the first person, because I have euthyroid autoimmune thyroiditis. Moreover, this autoimmune disorder has not only a deleterious impact on the serotonin system, but also on other important neurotransmitters, such as dopamine.

The Link Between Dopaminergic System and Euthyroid Autoimmune Thyroiditis

Even though it is believed that dopamine dysregulation is common in hypothyroidism, the dopaminergic system may be impaired by a condition of euthyroid autoimmune thyroiditis, as well.

Dopamine, indeed, is a crucial neurotransmitter that regulates emotions, stress resistance, sensation of pleasure and movements. It is mainly produced by neurons in the nigrostriatal region of the brain. It is thanks to dopamine if we can perform our daily tasks, walk and move our legs and hands.

Dopamine is produced by the synthesis of important amino acids, such as tyrosine. Hypothyroidism, but even autoimmune thyroiditis with normal thyroid hormones may upregulate the adsorption of essential and not essential amino acids, such as tryptophan and tyrosine, due to the gut problems that this ailment induces. Tyrosine allows the synthesis and production of dopamine in the adrenals and in the brain.

Moreover, the link between dopamine and thyroid diseases is confirmed by a study published in 2020 in the National Library of Medicine.

Dopaminergic system is interconnected with the hypothalamic-pituitary-thyroid axis.

Dopamine upregulates the release of TRH, the thyrotropin-releasing hormone, and downregulates TSH, the thyroid stimulating hormone. TRH is produced by neurons in the hypothalamus, which, in turn, stimulates the release of TSH and prolactin from the pituitary gland.

In a condition of chronic inflammation, this mechanism appears dysregulated over time and as the aforementioned study says, Thyroid disturbances, including hypothyroidism, Hashimoto’s thyroiditis (HT), hyperthyroidism and Graves’ disease (GD) not only increase the risk of Parkinson disease but also share some clinical signs with this neurological condition, such as tremors.

Euthyroid autoimmune thyroiditis is always an expression of a genetic vulnerability. If the altered gene is present, its negative effects may be triggered by a strict relation among environmental, social and psychological factors.

These bad effects and symptoms vary from mild anxiety to severe forms of bipolar disorder, and from neurological disturbances, such as brain fog, to brain diseases such as Parkinson’s.

Impact of Euthyroid Autoimmune Thyroiditis on the Gut

thyroid and gut

Usually, patients with autoimmune disorders have an alteration in the gut microbiota that may trigger food sensitivities and nutrient deficiencies, such as in vitamins of the group B, which, in turn, may cause depression and other mood disorders.

The alteration of gut microbiota is commonly caused by intestinal permeability or leaky gut. In this condition, the intestinal barrier is impaired and unable to protect the gastrointestinal trait from the passage of toxic substances. These substances enter the bloodstream, triggering the reaction of the immune system.

Leaky gut is often a reaction to stress, depression and unhealthy diet. Indeed, in euthyroid autoimmune disease, leaky gut is traditionally caused by the emotional dysregulation this condition entails. When you are stressed or depressed, the gut, which is the second brain, gets overstimulated and inflamed. In the gut, in fact, there is the habitat of the so-called enteric nervous system, which uses the same chemicals of the brain to digest food and alert the brain when something goes wrong.

That is the reason explaining why the emotional dysfunction of euthyroid autoimmune thyroiditis is always addressed towards these essential bodily organs. When you have this autoimmune disorder, you may also develop brain and gut dysfunctions. In short: even though you don’t become hypothyroid, you can experience brain or gut hypofunction over time, these conditions are more severe than a simple thyroid autoimmunity.

Moreover, emotional symptoms of euthyroid autoimmune thyroiditis escalates with aging and may cause the worst effects in menopausal women or during times of strong emotional stress, such as a pandemic.  This is another reason to understand the long-covid effects on euthyroid autoimmune patients. I am one of them. Those who are and were in this same condition reported severe depression, excruciating joint pain and extreme fatigue after the Covid infection.

Joint pain is always a symptom included in the list of thyroid disorders, and euthyroid autoimmune thyroiditis is not an exception. In euthyroid autoimmunity, osteoarticular inflammation is always linked to the emotional dysfunction in the brain and in the gut, even though the mainstream medicine says that it is a symptom of hypothyroidism. However, recent studies are trying to address the role of anti-thyroid peroxidase antibodies in inflammatory processes on other areas of the body, but this novel field requires additional studies to confirm it.


This article is based on my personal struggles with euthyroid autoimmune thyroiditis, and on authoritative medical research. However, nobody, so far, has taken care to discover and treat the true causes of this pathology. I hope you’ll never have symptoms, because this disease may remain asymptomatic for all life, with no harmful consequences. But, seeing that, in this stressful contemporary age, euthyroid autoimmunity is causing long-lasting symptoms, and, in addition, severe discomfort, I hope practitioners will be able to help us, sooner or later.

Someone will say to take selenium, but if you have a normal range (as I have) of this mineral, the effects on the brain and gut symptoms of your condition may be minimal.

Someone will say to remove your thyroid gland, but if you have a gene responsible for autoimmune diseases, you may develop other autoimmunities after the thyroid removal.

Finally, I really hope endocrinologists treat euthyroid autoimmune thyroiditis before it gives hypo or hyperthyroidism, but, above all, before it attacks your nervous system, especially the brain. Because, if so, it might be too late!

Author: Rosalba Mancuso
Rosalba Mancuso is a medical journalist, an international content writer credited at the University of Washington and a blogger born in Sicily. She is internationally appreciated for founding a network of four websites in English. On, Rosalba writes well researched and detailed health articles backed by her experience as a medical writer for pharma companies and as a PR assistant for a clinical analysis laboratory. She is also a member of the AHCJ, American Association of Health Care Journalists and Center for Excellence in Health Journalism. Her health magazine survives thanks to spontaneous donations, and sponsorships with brands and clinical organizations.